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Neurogenic Disorders > 6-7 > Flashcards

6-7 Flashcards

1
Q

Motor speech disorders include

A

Apraxia & dysarthria

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2
Q

Types of apraxia of speech

A

Dyspraxia
Aphemia
Peripheral motor aphasia
Apraxic Dysarthria

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3
Q

To act or move

A

Praxis

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4
Q

A mean -

A

Without

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5
Q

Apraxia means: to not _____ per to not ___

A

To not act or to not move

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6
Q

Apraxia means lack of movement or action for speech production

A
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7
Q

Various kinds of apraxia

A

Inability to move eyes, limbs, and structures

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8
Q

An acquired disorder of speech originating from an inability to create and sequence motor plans for speech

A

Apraxia of speech

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9
Q

Apraxia of speech May co-occur with dysarthria. True or false

A

True

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10
Q

Apraxia of speech Usually co-occurs with some kind of aphasia . True or false

A

True

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11
Q

Common that a person has apraxia of speech without some language impairments. Tue or false

A

False. Rare that a person has apraxia of speech without some language impairments

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12
Q

Apraxia of speech; Rooted in an inability to ______the neural impulses necessary to create appropriate motor movements for speech

A

Rooted in an inability to create and sequence (program) the neural impulses necessary to create appropriate motor movements for speech

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13
Q

Apraxia of speech Construction of appropriate motor plans for movements of the articulators to produce non-speech actions are unaffected.

A
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14
Q

Not a single structure in the CNS, but a network of structures that all contribute to the function of putting together appropriate motor plans for speech.

A
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15
Q

Certain left hemisphere structures play a large role
For apraxia of speech

A
  1. Broca’s area and supplementary motor cortex
    2.Primary motor cortex, basal ganglia, and cerebellum
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16
Q

Characteristics of Apraxia of Speech

A

Effortful speech
Aware of speech errors
Self-repairs
Struggle and frustration

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17
Q

Characteristics of Apraxia of Speech Cont.

A

Limited prosody
Slowed rate- to avoid errors
Inconsistent errors- Islands of intact speech
Visible, auditory groping of the tongue, lips, and mandible
Resonance, respiration coordination, and phonation left relatively intact

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18
Q

Articulation errors Usually occur on the ____ phoneme

A

Usually occur on the first phoneme

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19
Q

The more ___ the word, the more likely an error will occur

A

Complex

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20
Q

Articulation errors

A

Consonant clusters of /l/ and /s/

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21
Q

Common articulation errors in apraxia of speech

A

Usually occur on the first phoneme
The more complex the word, the more likely an error will occur
Consonant clusters of /l/ and /s/
Might produce different error patterns on the same word
Phoneme substitutions and distortions

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22
Q

Articulation errors cont.

A

Perseverative substitutions
Anticipatory substitutions
Phoneme additions
Phoneme prolongations
Voicing errors

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23
Q

Damage to the left hemisphere at or around —________

A

Inferior posterior frontal lobe

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24
Q

Etiologies of apraxia of speech

A

Any process or event that damages the left inferior-posterior frontal lobe

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25
Q

Etiologies of apraxia of speech

A

Any process or event that damages the left inferior-posterior frontal lobe
Usually stroke involving occlusion of the left middle cerebral artery
Generalized head trauma
Focal head trauma- surgical removal of tumor or aneurysm near Broca’s area

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26
Q

A neurodegenerative condition in which patients display a slow onset of apraxia of speech that gains in severity over time as a result of continued atrophy of the lateral premotor cortex and the supplementary motor area

A

Primary progressive apraxia of speech

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27
Q

Evolves into a condition of degeneration of
-The premotor cortex, prefrontal cortex, primary
-Motor cortex, basal ganglia, midbrain, and corpus callosum

A

Primary progressive apraxia of speech

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28
Q

Inability to program and carry out any volitional movements of the tongue, lips, pharynx, or larynx on command

A

Buccofacial Oral Apraxia
A.K.A. noverbal apraxia or oral apraxia

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29
Q

May be able to move articulators in a natural context, though not on command

A

Oral apraxia

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30
Q

Volitional speech can be affected, with more formulaic and automatic utterances left unimpaired

A

Oral apraxia

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31
Q

Inability to program motor movements for the use of tools and the pantomiming of gestures despite possessing the knowledge of how the object is used and its function

A

Ideomotor apraxia

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32
Q

May be able to explain the purpose and how to use a hairbrush, but cannot complete the task on command (though can complete the task in a natural context)

A

Ideonotor apraxia

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33
Q

Inability to:
Conceptualize a task
Formulate motor plans required for the task
Hold the idea of the task long enough to accomplish the task successfully

A

Ideational apraxia

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34
Q

May be able to perform individual components of a task, but cannot perform the series of actions sequentially to accomplish the entire act
Raise a hairbrush to their head, but unable to accomplish the remaining actions necessary
Cannot perform the task volitionally or automatically

A

Ideational apraxia

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35
Q

Concomitant disorders of apraxia of screech

A

Hemiplegia or hemiparesis
Hyperflexia
Dysarthria
Buccofacial oral apraxia/ideomotor apraxia
Nonfluent aphasia

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36
Q

Contralateral to the lesion
Usually affects written language by weakening dominant writing hand, while the apraxia of speech affects verbal output of language

A

Hemiplegia or hemiparesis

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37
Q

Extrapyramidal impulses of reflex regulation unable to reach the brainstem and spinal cord
Damage to the upper motor neurons with transmit extrapyramidal impulses of reflex regulation to the brain stem and spinal cord.

A

Hyperflexia

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38
Q

Articulation errors occur more often on longer/complex words
Errors are varied and inconsistent
More difficulty producing volitional than reflexive automatic utterances
Buccofacial-oral apraxia more likely
Normal muscle strength, muscle tone, and appropriate ROM

A

Apraxia

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39
Q

Articulation errors occur on all words in all utterances
Errors are consistent and predictable
Buccofacial-oral apraxia less likely
Impaired oral/ velopharyngeal muscle strength, abnormal muscle tone, and limited ROM

A

Dysarthria

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40
Q

The presence of motor speech disorders often implies a problem with the nervous system, which may validate a medical-neurological disease.

A
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41
Q

Components of evaluation

A

Identification of confirmatory signs to support hypothesized motor speech diagnosis
Instrumental measures
Administration of a formal test of apraxia of speech, dysarthria, and/or speech intelligibility

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42
Q

Examination of the patient’s individual oral structures and articulators, and observation of nonspeech functions of these structures

A

Eval

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43
Q

Tests patient’s maximum limit of ability by comparing patient’s greatest effort on a task with the known average performance rate of unimpaired individuals

A

Maximum performance task

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44
Q

Alternating motion rates (AMRs)
Simple repetitive motor tasks used to test speed and regularity

A

Diadochokinetic rates (DDKs)

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45
Q

Rapid repetition of more than one syllable at a time to test ability to rapidly move articulators successfully and precisely

A

Sequential motion rates (SMRs)

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46
Q

Types. Of maximum performance tasks

A

Diadochokinetic rates (DDKs)
Sequential motion rates (SMRs)

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47
Q

Patient produces continuous speech for at least 5 minutes.
-See if person becomes fatigued
-See how fatigue affects speech

A

Speech stress test

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48
Q

If speech degrades over 5 minutes or less due to fatigue, this is indicative of _-__

A

If speech degrades over 5 minutes or less due to fatigue, this is indicative of pathology

49
Q

Speech tasks include

A

Verbal repetitions of words, phrases, and sentences
Oral reading tasks of various length

50
Q

Patient’s ability to produce connected and spontaneous speech is appropriately assessed:
Asking open-ended questions
Verbally describing a picture presented
Telling or retelling of a story

A
51
Q

No pharmaceuticals or prosthetics are used to treat Apraxia.

A
52
Q

Three therapy treatment approaches to treat apraxia of speech:

A

Three therapy treatment approaches:
Articulatory kinematic therapy
Intersystemic reorganization
Alternative/augmentative communication strategies

53
Q

Relies on motor learning theory and neuroplasticity to re-establish motor planning abilities for speech

A

Articulatory kinematic s approach

54
Q

Lost motor abilities can be retrieved or rebuilt by cueing the brain to produce or access the motor plans despite brain damage

A

Articulatory kinematic app rich

55
Q

_____ relies on three components:
1. Motor practice
2. Middling repetition
3. Articulatory cueing

A

Articulatory kinematic s approach

56
Q

Intensive and repetitive production of target phonemes in isolation or within words or phrases to increase articulatory ability

A

Motor practice

57
Q

Intensive and repetitive production of target phonemes in isolation or within words or phrases to increase articulatory ability

A

Modeling repetition

58
Q

Phonetic placement descriptions given by SLP to increase patient’s awareness and understanding of articulatory movements needed to produce the target word

A

Articulatory queuing

59
Q

Provides tactile kinesthetic, visual, and auditory cues to elicit production of target phoneme

A

Phonemes for Restructuring Oral Muscular Phoneme Targets (PROMPT)

60
Q

PROMPT Uses touch and motion cues to the patient’s head, face, or neck at different points to illustrate:

A

lace of articulation
Muscles used for phoneme production
Level of tension in muscles
Voicing
Nasality
Movement of articulators
Timing/speech of movement
Degree of opening mandible

61
Q

Capitalizes on a patient’s intact ability to produce melody in spite of loss of speech

A

Melodic intonation therapy

62
Q

Pairing a physical act (gesture) not previously paired with speech with the simultaneous production of a target word

A

Intersystemic reorganization

63
Q

Only used for long-term use with those who have severe or profound levels of apraxia of speech

A

Augmentative and alternative strategies

64
Q

Group of disorders produced by damage to the CNS or PNS, which results in disordered movement that affects speech production

A

Dysarthria

65
Q

Each dysarthria has its own specific profile of speech and physiological characteristics that are the result of the site of damage in the CNS or PNS

A
66
Q

Dysarthria types

A

Flaccid
Spastic
Unilateral upper motor neuron
Ataxic
Hypokinetic
Hyperkinetic
*Mixed

67
Q

On one side q

A

Unilateral

68
Q

On both sides

A

Bilateral

69
Q

On the same side q

A

Ipsilateral

70
Q

On the opposite side

A

Contralateral

71
Q

Partial or incomplete loss of movement (weakness)

A

Paresis

72
Q

Total loss of movement

A

Paralysis

73
Q

Abnormal change in body tissue, usually as a result of disease or trauma

A

Lesion

74
Q

Systems supporting the production of speech, which includes articulatory, phonatory, and respiratory systems

A

Speech systems

75
Q

lack of appropriate muscle tone

A

Hypotonic

76
Q

excess/tightness of muscle tone

A

Hypertonic

77
Q

L ack of appropriate reflexes

A

Hypo reflex ia

78
Q

excess/overactive reflexes

A

Hyper reflex ia

79
Q

Lack of appropriate level of movement

A

Hypokinetic

80
Q

excess or too much movement to be appropriate

A

Hyperkinetic

81
Q

Results from flaccid weakness or paralysis of musculature used to produce speech
Created by low muscle tone (hypotonia) and weakness in the muscle

A

FLACCID dysarthria

82
Q

Ethnologies of flaccid dysarthria

A

Created by damage to the LMNs of the cranial nerves or to connections between LMNs and muscle fibers
Infections
Autoimmune/neurodegenerative diseases
Surgical trauma
Tumor
Toxins
Mass effect
Congenital syndromes
Brainstem stroke to cranial nuclei

83
Q

Damage to lower motor neurons (LMNs) of the cranial nerves
Typically seen in

A

Flaccid dysarthria

84
Q

Damage to LMNs of cranial nerves is usually where they synapse at the brainstem at the cranial nerve nuclei

A

Flaccid dysarthria

85
Q

Trigeminal nerve damage has three branches:

A

Has three branches
Ophthalmic: sensory branch
Maxillary: sensory branch
Mandibular: motor to mandible

86
Q

Lesion to right or left nerve will weaken/disable corresponding side of the mandible

A

Unilateral trigeminal nerve damage

87
Q

Contralateral and undamaged side of the mandible still functional

A

Unilateral trigeminal nerve damage

88
Q

Mandible will deviate toward side of damage

A

Unilateral trigeminal nerve damageq

89
Q

Both right and left nerve damage weakens or paralyzes the right and left side of mandible

A

Bilateral trigeminal nerve damage

90
Q

May be unable to raise mandible for articulation or mastication purposes

A

Bilateral traigmental nerve damage

91
Q

Facial never damage divided in 4 branches

A

Divided into four branches:
Temporal: innervates muscles around eyes and movement of forehead for facial expression
Buccal: innervate muscles of the lower face to control lips and compression of cheeks
Zygomatic: innervate muscles of the lower face to control lips and compression of cheeks
Mandibular: innervate muscles of the lower face to control lips and compression of cheeks

92
Q

Inability to move muscles of the face from lesion that occurs before division of nerve

A

Unilateral facial nerve damage

93
Q

Unilateral lesion will decrease motor function ipsilaterally

A

Unilateral facial nerve damage

94
Q

Facial asymmetry will be present
:

A

Facial asymmetry will be present
Weakened side of the lips will sag below unaffected side of the lips
Air will leak from affected side of the lips when inflating cheeks
Difficulty blinking affected eye and/or ptosis (droopy eyelid) may occur on affected side
On the affected side of the face, the eyebrow will have decreased range of motion and forehead will be smooth and unwrinkled

95
Q

Articulation of phonemes requiring strong labial seal may be mildly impaired

A

Unilateral facial nerve damage

96
Q

Bilateral facial weakness
May be unable to bring lips together at all
Cannot produce bilabial or labiodental phonemes

A

Bilateral facial nerve damage

97
Q

Courses through head and neck before moving into thorax
Branches of vagus innervate many important structures for speech

A

Vargas nerve damage

98
Q

Innervates muscles of pharynx and velum
Weakness on ipsilateral side of pharynx and velum with contralateral function intact

A

Unilateral Vargas nerve to the pharyngeal plexus

99
Q

Damage to right and left pharyngeal plexuses

A

Bilateral vagus nerve damage to the pharyngeal plecxus

100
Q

Passes under subclavian artery on the right and under the aorta on the left to course back up superioriorly to innervate all intrinsic muscles of the larynx (except cricothyroid)

A

Unilateral recurrent laryngeal nerve damage

101
Q

Vocal folds paralyzed at midline
Unable to approximate for phonation
Respiration may be difficult

A

Bilateral recurrent laryngeal nerve damage

102
Q

Innervates intrinsic and extrinsic muscles of the tongue (except palatoglossus)
Unilateral damage causes weakness on side of tongue ipsilateral to lesion

A

Unilateral hypoglossal nerve damage

103
Q

Bilateral lingual weakness
Difficulty protruding the tongue
Reduced lingual range of motion

A
104
Q

Confirmatory signs of Flaccid Dysarthria

A

Lower motor neuron damage may result in
Hypotonia
Muscle atrophy
Fasciculations
Hyporeflexia

105
Q

Created by spasticity in muscles associated with speech production

A

Spastic dyarthria

106
Q

Upper motor neurons (UMNs) are descending (efferent) tracts of axons that begin in cerebral cortex and travel within the CNS to synapse with LMNs of PNS

A

Spastic dysarthria

107
Q

Origin of spastic dysarthria is bilateral damage to UMNs

A

Q

108
Q

Confirmatory signs of Spastic Dysarthria

A

Bilateral UMN damage creates:
Hypertonia
Hyperreflexia

109
Q

Lesion bilaterally to the UMNs will create effects seen on both sides of the body

A

Spastic dysarthria

110
Q

Incoordination
Produces a slushy or drunken-like speech quality
Imprecise production of consonants, excess and equal stress, and irregular articulatory breakdowns

Weakness will not be present
All oral and facial structures will appear normal at rest
Signs appear only during movement

A

Ataxic dysarthria q

111
Q

Result of pathology of the cerebellum
Responsible for monitoring and correcting errors in timing, range, force, and direction of motor movements in the motor plan

A

Ataxic dysphasia q

112
Q

Confirmatory signs of Ataxic Dysarthria

A

Not confined to speech production alone
May display signs of decreased cerebellar functioning in addition to ataxic dysarthria
Ataxic gait
Dysmetria

113
Q

Over- or undershooting the of the movement of a body part while performing a volitional movement

A

Dysmetria q

114
Q

Feet usually spread broadly apart, with irregular foot steps and a greater likelihood of falls

A

Ataxic gait q

115
Q

Result of pathology at the basal ganglia or its connections to other structures in CNS
Neuromotor basis is rigidity, reduced amounts of volitional movement, and reduced range of motion in the movement remaining

A

Hyperkinetic dysarthria

116
Q

Movements of structures of speech systems become erased entirely or reduced in range of motion

A

Hpokinetic dysarthria q

117
Q

Damage to structures of the basal ganglia or the connections between the structures of the basal ganglia and other CNS structures

A

Hypokinetic dysarthriaq

118
Q

Damage creates rigid muscle tone, postural abnormalities, difficulties initiating movement, deficits in ability to learn new motor movements, and tremors at rest

A

Hypokinetic dysartihea q

Neurogenic Disorders (5 decks)

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